RESUMO
Store-operated channels activated in response to intracellular calcium store depletion represent the main pathway of calcium entry from the extracellular space in nonelectroexcitable cells. Adapter proteins organize the components of this system into integral complex. We studied the influence of adapter proteins of the Homer family on endogenous store-operated calcium Imin channels in A431 cells. Monomeric Homer 1a proteins increase activity of Imin channels, but did not modulate their electrophysiological properties. Recombinant Homer 1c protein did not block the induced calcium currents.
Assuntos
Canais de Cálcio/metabolismo , Cálcio/metabolismo , Proteínas de Arcabouço Homer/fisiologia , Potenciais de Ação/efeitos dos fármacos , Agonistas dos Canais de Cálcio/metabolismo , Agonistas dos Canais de Cálcio/farmacologia , Canais de Cálcio/efeitos dos fármacos , Canais de Cálcio/fisiologia , Sinalização do Cálcio/efeitos dos fármacos , Citoplasma/metabolismo , Fenômenos Eletrofisiológicos/efeitos dos fármacos , Proteínas de Arcabouço Homer/farmacologia , Humanos , Ativação do Canal Iônico/efeitos dos fármacos , Técnicas de Patch-Clamp , Multimerização Proteica/fisiologia , Proteínas Recombinantes/farmacologia , Células Tumorais CultivadasRESUMO
An important role in intracellular calcium signaling is played by store-operated channels activated by STIM proteins, calcium sensors of the endoplasmic reticulum. In stable STIM1 knockdown HEK S4 cells, single channels activated by depletion of intracellular calcium stores were detected by cell-attached patch-clamp technique and their electrophysiological parameters were described. Comparison of the properties of single channels in HEK293 and HEK S4 cells revealed no significant differences in their current-voltage curves, while regulation of store-operated calcium channels in these cell lines depended on the level of STIM1 expression. We can conclude that electrophysiological peculiarities of store-regulated calcium entry observed in different cells can be explained by differences in STIM1 expression.